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The vascular contribution to Alzheimer's disease
Abstract
AD (Alzheimer's disease) is a progressive neurodegenerative disease of unknown origin. Despite questions as to the underlying cause(s) of this disease, shared risk factors for both AD and atherosclerotic cardiovascular disease indicate that vascular mechanisms may critically contribute to the development and progression of both AD and atherosclerosis. An increased risk of developing AD is linked to the presence of the apoE4 (apolipoprotein E4) allele, which is also strongly associated with increased risk of developing atherosclerotic cardiovascular disease. Recent studies also indicate that cardiovascular risk factors, including elevated blood cholesterol and triacylglycerol (triglyceride), increase the likelihood of AD and vascular dementia. Lipids and lipoproteins in the circulation interact intimately with the cerebrovasculature, and may have important effects on its constituent brain microvascular endothelial cells and the adjoining astrocytes, which are components of the neurovascular unit. The present review will examine the potential mechanisms for understanding the contributions of vascular factors, including lipids, lipoproteins and cerebrovascular Aβ (amyloid β), to AD, and suggest therapeutic strategies for the attenuation of this devastating disease process. Specifically, we will focus on the actions of apoE, TGRLs (triacylglycerol-rich lipoproteins) and TGRL lipolysis products on injury of the neurovascular unit and increases in blood–brain barrier permeability.
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Several vascular risk factors, including the apoE-LDLR system, are shared by AD and CVD.
“In addition, several vascular risk factors, including apoE-LDLR system, are shared by AD and CVD (Altman et al., 2010).”
From Apolipoprotein E–low density lipoprotein receptor interaction affects spatial memory retention and brain ApoE levels in an isoform-dependent manner (2014) · cites this paper as Altman et al., 2010
The Conclusions report overlapping risk factors for AD and atherosclerotic cardiovascular disease, including dyslipidaemia and the apoE4 allele. The APOE STRUCTURE AND FUNCTION section says apoE interacts with LDL receptors, but does not identify the apoE–LDLR system as a shared risk factor; that specific example goes beyond what the paper states. Page numbers are unavailable in our copy. (LLM, conf=0.86)
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Metadata
- Authors
- Altman, R., & Rutledge, J. C.
- Affiliations
- Department of Internal Medicine, University of California Davis, 451 East Health Sciences Drive, Davis, CA 95616, U.S.A.
- Venue
- Clinical Science
- Publisher
- Portland Press Ltd.
- Published
- 2010-08-05
- Volume
- 119
- Issue
- 10
- Pages
- 407-421
- ISSN
- 0143-5221
- 1470-8736
- PMC
- PMC2950620
- Cited by
- 93
- References
- 24
- Language
- en
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